ライフサイエンスコーパス: microsatellite stable

1 rosatellite unstable) or non-Lynch syndrome (microsatellite stable).

2 tely differentiated invasive adenocarcinoma, microsatellite stable.

3 d in the context of biallelic mutations were microsatellite stable.

4 , in all cases the matched breast cancer was microsatellite stable.

5 All 13 FGPs were microsatellite stable.

6 All of the other tumors were considered microsatellite stable.

7 Of the 209 cases, 65% cancers were microsatellite stable, 21% were MSI-low, and 14% were MS

8 ctal cancers were divided into 4 groups: (1) microsatellite stable, Amsterdam-positive (MSS HNPCC) (N

9 t colorectal (and other) cancers, and having microsatellite stable and unstable tumors were included.

10 The remaining 80% to 85% of CRCs are microsatellite stable but most are characterized by chro

11 tion, the tumors from mutation carriers were microsatellite stable but tended to acquire base substit

12 and 43% of MSI colon cancers, but only 7% of microsatellite stable cancers.

13 re the best discriminators between MSI-H and microsatellite-stable cancers (odds ratio: 37.8, 9.8, an

14 Retention of 18q alleles in microsatellite-stable cancers and mutation of the gene f

15 We also found that 37.8% of microsatellite-stable cancers had no LOH events identifi

16 le cell lines and constitutive expression in microsatellite-stable cell lines.

17 NonRER (microsatellite stable) cell lines typically displayed hi

18 e resistant to 5-FU in culture compared with microsatellite stable cells, despite similar amounts of

19 esenchymal phenotype and invasiveness of the microsatellite-stable CoLo741 cells (which express endog

20 d methylator phenotype (CIMP), especially in microsatellite stable colon cancer, is not accepted univ

21 as acquired somatic mutations in a set of 30 microsatellite stable colon tumors.

22 We conclude that the BRAF V600E mutation in microsatellite-stable colon cancer is associated with a

23 osomal protein can predispose individuals to microsatellite-stable colon cancer.

24 better patient survival rates compared with microsatellite stable colorectal cancer.

25 he rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tum

26 In the majority of microsatellite-stable colorectal cancers (CRCs), an init

27 her proportion of susceptibility to sporadic microsatellite-stable CRC than previously assumed.

28 r, respectively, in adenomas associated with microsatellite-stable CRC versus microsatellite-unstable

29 ression different from those associated with microsatellite-stable CRC, and demonstrate that p12(DOC-

30 netic, and epigenetic features distinct from microsatellite-stable CRC.

31 ffer significantly from those observed among microsatellite-stable CRC.

32 the recently described group of hypermutant, microsatellite-stable CRCs is likely to be caused by som

33 S phase and decreased apoptosis compared to microsatellite-stable (DOC-1+) cell lines.

34 that 8-oxoG levels were elevated in several microsatellite stable human colorectal cancer cell lines

35 f sporadic CRCs and underlie a hypermutator, microsatellite-stable molecular phenotype.

36 MSI, defined as MSI high (MSI-H) or MSI-low/microsatellite stable (MSI-L/MSS), was assessed in tumor

37 satellite instability (MSI-positive) and 107 microsatellite stable (MSI-negative) tumors.

38 The distinction between microsatellite stable (MSS) and low frequency MSI (MSI-L

39 icrosatellite instability and those that are microsatellite stable (MSS) but chromosomally unstable.

40 istinct gene expression profiles for MSI and microsatellite stable (MSS) cancers, which suggest that

41 compared with both wild-type cell lines and microsatellite stable (MSS) cell lines.

42 otility, and invasion consistent with EMT in microsatellite stable (MSS) colon cancer cells, whereas

43 Among microsatellite stable (MSS) colon cancers, we now find t

44 T genotype were more likely to have MSI than microsatellite stable (MSS) CRC [odds ratio (OR) 1.90; 9

45 the potential role of mutator phenotypes in microsatellite stable (MSS) CRC carcinogenesis.

46 microsatellite instability (MSI), but not in microsatellite stable (MSS) CRC cell lines and tumors.

47 and the best diagnostic approaches to detect microsatellite stable (MSS) HNPCC tumors are unclear.

48 nstability (CIN) is a major driving force of microsatellite stable (MSS) sporadic CRC.

49 All 54 MSI-H colon cancers and 20 random microsatellite stable (MSS) tumors from a population-bas

50 stability (MSI-H) sporadic CRCs, its role in microsatellite stable (MSS) tumors is debated.

51 ts reveals 24 significantly mutated genes in microsatellite stable (MSS) tumours and 16 in microsatel

52 Of these, 680 were microsatellite stable (MSS), 27 were MSI-H, and 111 were

53 C, three tumor phenotypes have been defined: microsatellite stable (MSS), low-frequency MSI, and high

54 colorectal tumors and characterized them as microsatellite stable (MSS), MSI high or MSI low, CIMP h

55 chromosomal instability (CIN); herein termed microsatellite stable (MSS).

56 of those that were not infected with EBV and microsatellite stable (MSS).

57 In the subgroups of MSI-H and microsatellite stable (MSS)/low-frequency MSI (MSI-L) tu

58 henotypes (GMPs) underlying MSI-H, MSI-L, or microsatellite-stable (MSS) tumors have never been evalu

59 le (MSI) tumors, as well as in a subgroup of microsatellite-stable (MSS) tumors.

60 trial cancer based on microsatellite status (microsatellite-stable (MSS) vs. microsatellite-instable

61 tation, negative for KRAS mutation); type 2 (microsatellite stable [MSS] or MSI-low, CIMP-positive, p

62 nstability (MSI) and chromosome instability (microsatellite stable; MSS), are best understood in the

63 Microsatellite-stable, near-diploid (MSI-CIN-) colorecta

64 tric tumorigenesis, including both MSI-H and microsatellite-stable neoplasms.

65 vant therapy compared with patients who have microsatellite-stable or proficient mismatch repair (pMM

66 ethylation existed in sporadic CRCs (MSI and microsatellite stable) or normal colonic tissues.

67 The genomic anomaly frequencies observed in microsatellite stable PDX reproduce those detected in no

68 %) of MSI CRC cell lines, but in none of the microsatellite stable samples (0/12).

69 Among patients with microsatellite-stable stage III cancer, five-year overal

70 All POLE EDM tumours were microsatellite stable, suggesting that defects in either

71 All four tumors were microsatellite stable; three had IHC staining patterns c

72 s associated with KRAS mutation (P = 0.033), microsatellite stable tumors (P = 0.015), decreased expr

73 In a multivariate analysis of microsatellite stable tumors, CIMP high was related sign

74 st, no frameshift mutations were found in 70 microsatellite stable tumors.

75 umors (19.1% of MSI-H versus 2.2% of MSI-low/microsatellite stable tumors; P = 0.002).

76 SI (541 [146-8063]; P < .001), and lowest in microsatellite-stable tumors (70.5 [7-1877]; P < .001).

77 rs, but only 8% of MSI-low tumors and 13% of microsatellite-stable tumors (P=0.0001).

78 BRAF mutation was seen in 5% (40 of 803) of microsatellite-stable tumors and 51.8% (43 of 83) of mic

79 ted with shorter DFS and OS in patients with microsatellite-stable tumors but not in patients with MS

80 tern of MS indels can accurately distinguish microsatellite-stable tumors from tumors with microsatel

81 he subgroup analysis showed in patients with microsatellite-stable tumors that both KRAS (HR for DFS:

82 In microsatellite-stable tumors, this mutation was related

83 ith Lynch syndrome, MLH1-hypermethylated, or microsatellite-stable tumors.

84 ifies a previously unrecognized mechanism in microsatellite-stable tumors.

85 (32.8 vs 13.5; P < .001) TILs compared with microsatellite-stable tumors.

86 uished MSI-H from non-MSI-H (i.e., MSI-L and microsatellite stable) tumors and was designated the MSI

87 in less than 10% of loci were classified as microsatellite stable, whereas MSI was diagnosed in case